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目的 探讨脑胶质瘤中p16基因CPG岛甲基化与该基因失活的相关性。方法 应用免疫组化检测 5 0例脑胶质瘤中p16蛋白的表达 ;应用PCR技术检测脑胶质瘤中p16基因第 1、2外显子缺失及第 1外显子 5’ CPG岛高甲基化。结果 免疫组化结果显示 5 0例脑胶质瘤组织中p16蛋白表达阳性者 2 3例 ;p16蛋白表达阴性者 2 7例 ,基中p16基因纯合性缺失者 9例 ,p16基因CPG岛高甲基化者 7例。结论 恶性脑胶质瘤中p16蛋白表达缺失而没有p16基因纯合性缺失 ,是由于p16基因 5’端CPG岛高甲基化后抑制该基因的转录所致。p16基因高甲基化也是该基因失活的重要机制之一。
Objective To investigate the relationship between methylation of p16 gene CPG island and inactivation of this gene in gliomas. Methods The expression of p16 protein in 50 gliomas was detected by immunohistochemistry. The deletion of exon 1 and exon 1 of p16 gene and hypermethylation of exon 1 in 5 glioma were detected by PCR . Results The results of immunohistochemistry showed that there were 23 cases with positive p16 protein in 50 cases of glioma, 27 cases with negative p16 protein, 9 cases with homozygous deletion of p16 gene in base, In 7 cases. Conclusions The deletion of p16 protein in malignant gliomas without the loss of homozygosity of p16 gene is due to the hypermethylation of the 5 ’end of p16 gene, which inhibits the transcription of this gene. Hypermethylation of p16 is also one of the important mechanisms of inactivation of this gene.